MOST POPULAR ARTICLES OF THE MONTH

Editor's Note

“You can’t cure me, ’cause there ain’t nothing wrong with me!!” If I only had a dollar for every time one of my patients told me this. What makes these ridiculous statements even harder to believe is that many patients will do everything properly to take care of themselves, and then it is like the “Men in Black” flash their memory gadget, and suddenly the patients totally forget they ever had diabetes. This week our disaster avoided looks at one of these patients.

Dave Joffe

Editor-in-chief

DISASTERS AVERTED — Near Miss Case Studies

Woman, 64 years of age. History of Class II Obesity and hyperlipidemia. While she had obesity, her glucose levels were elevated. A1C 8.2%. She followed a lower carb meal plan, was active, took metformin and a GLP-1, a statin and an ACE-I. She lost 22% total body weight. A1C then remained in the 6-6.5% range for 3 years on this treatment plan. Over the past 8 months, due to insurance and her statement of denial that she ever really had diabetes, she stopped taking her glucose-lowering medication, statin, and ACE-I, wasn’t as strict with meal plan or activity, and stopped checking her glucose, but did not gain back her weight.

EXCLUSIVE INTERVIEW — Candid Video Interviews with Top Practitioners

Dr. Yehuda Handelsman talks with Diabetes in Control Publisher Steve Freed at the 2016 AACE Meeting. In part 3 of this Exclusive Interview, Dr. Handelsman explains how he prioritizes medications/lifestyle changes when treating diabetes and managing various co-morbidities.

CLINICAL GEMS — The Best from Diabetes Texts

Sympathetic effects and mediation: Sympathetic nerves inhibit insulin and stimulate glucagon secretion. Their activation may help mediate stress-induced changes in islet hormone secretion including the glucagon counterregulatory response to hypoglycemia.These effects may be mediated by the combination of the classical neurotransmitter noradrenaline and the sympathetic neuropeptides (galanin and NPY). All three neurotransmitters can inhibit insulin and stimulate glucagon secretion, thus mimicking the effects of sympathetic activation on islet hormone secretion. In addition, galanin and NPY meet several other of the criteria needed to be classified as a physiologic neurotransmitter.

College student, type 1 diabetes, wears a pump and CGM. She has good family support. Several of her family members get her CGM readings on their phone. She received a call from her mother about 2:45 am waking her up. She told her to treat her low blood glucose, which patient reported to be 41.

MOST POPULAR ARTICLES OF THE MONTH

“You can’t cure me, ’cause there ain’t nothing wrong with me!!” If I only had a dollar for every time one of my patients told me this. What makes these ridiculous statements even harder to believe is that many patients will do everything properly to take care of themselves, and then it is like the “Men in Black” flash their memory gadget, and suddenly the patients totally forget they ever had diabetes. This week our disaster avoided looks at one of these patients.

Woman, 64 years of age. History of Class II Obesity and hyperlipidemia. While she had obesity, her glucose levels were elevated. A1C 8.2%. She followed a lower carb meal plan, was active, took metformin and a GLP-1, a statin and an ACE-I. She lost 22% total body weight. A1C then remained in the 6-6.5% range for 3 years on this treatment plan. Over the past 8 months, due to insurance and her statement of denial that she ever really had diabetes, she stopped taking her glucose-lowering medication, statin, and ACE-I, wasn’t as strict with meal plan or activity, and stopped checking her glucose, but did not gain back her weight.

Dr. Yehuda Handelsman talks with Diabetes in Control Publisher Steve Freed at the 2016 AACE Meeting. In part 3 of this Exclusive Interview, Dr. Handelsman explains how he prioritizes medications/lifestyle changes when treating diabetes and managing various co-morbidities.

Sympathetic effects and mediation: Sympathetic nerves inhibit insulin and stimulate glucagon secretion. Their activation may help mediate stress-induced changes in islet hormone secretion including the glucagon counterregulatory response to hypoglycemia.These effects may be mediated by the combination of the classical neurotransmitter noradrenaline and the sympathetic neuropeptides (galanin and NPY). All three neurotransmitters can inhibit insulin and stimulate glucagon secretion, thus mimicking the effects of sympathetic activation on islet hormone secretion. In addition, galanin and NPY meet several other of the criteria needed to be classified as a physiologic neurotransmitter.

College student, type 1 diabetes, wears a pump and CGM. She has good family support. Several of her family members get her CGM readings on their phone. She received a call from her mother about 2:45 am waking her up. She told her to treat her low blood glucose, which patient reported to be 41.